ESSENTIAL PATHOLOGY
Year 2 Sem 1
Practical 4
Atherosclerosis
General gross description
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an intimal lesion, made up of a deposition of fats, cholesterol`l esters, necrotic debris and
foam cells with a variable chronic fibrotic inflammatory response forming a superficial
fibrous cap containing smooth muscle and foam cells and lymphocytes
complications are ulcers with ulcers with thrombi, bleeding into plaque, embolization of
thrombi and/or atheroma, calcifications and atrophy of media with formation of aneurysm
thickening of
intima layer
Ruptured
plaque
Lumen
Advanced plaque
note the discrete intimal nodulae thickening the arterial wall, obstruction of lumen and
ruptures of atheromatous plaque
the increased cellularity is made up of both fibroblasts and smooth muscle cells
the proliferation of these cells is a major component of the genesis of the atherosclerotic
plaque
field shows atheromatous plaque in intima layer
The more deeply pinker staining right upper portion of the field is the sclerotic fibrous
cap. the lighter stain elsewhere is due to deposition of neutral fats which are washed out
by the tissue processing for slide preparation
note the slit like clear spaces which were occupied by washed out cholesterol esters
crystals before processing
the fine blue stipples throughout are calcific spherules
the high magnification the atheroma shows numerous foam cells and an occational
cholesterol cleft. a few dark blue inflammatory cells are scatter within the atheroma.
Foam cells filled with lipid appear as large, pale staining cells very vacuolated cytoplasm.
These cells may derive form myointimal cells or macrophage. As the lesion progress
some of the foam cells break down and liberate free lipid into the intima where it is
represented by non staining angular clefts.
Question
1. Draw and describe the histopathological changes of the given slide
2. Explain the pathogenesis of atheroma formation
3. Discuss the sequelae of atherosclerosis
Myocardial Infarct
General Gross Description
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early acute MI
note the copious exudates of neutrophils (PMN) between the muscle fibers
note the absence of nuclei in the myocardial fibers indicating necrosis, eg infarction
PMNs have a life span of 24 hours and then undergo karyorrhexis which is not seen here
suggesting that this lesion is less than 2 days old.
Healing acute MI
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capillaries, elongate fibroblast nuclei, collagen fibrils and macrophages all typical
components of granulation tissue can be seen
macrophages can be seen containing a dark pigment which is probably hemosiderin
because of the color and variation in particle size
the rest, wave fibers are collagen and represent the scar tissue that will ultimately replace
the dead myocardium
Questions
1. Draw and describe the histopathological changes of the given slide
2. Identify the stage of infarction.
Cirrhosis of liver
Cirrhosis is the end result of continued damage to liver cells from a great many causes. It is
characterized by wholesale disruption of the liver architecture and the formation of nodules of
regenerating liver cells separated by fibrous band. There are two main effects of this altered liver
architecture and cellular damage namely disturbance of blood flow through the liver from portal
vein to hepatic vein. The classification of cirrhosis is based on the disease which causes the
underlying liver damage. The most important causes are chronic alchol abuse, chronic hepatitis
and biliary cirrhosis. In small percentage of cases no underlying disease can be found: this is
known as cryptogenic cirrhosis.
broad fibrous bands connecting portal areas and intervening nodules of liver cells
marked fatty changes
Cryptogenic cirrhosis
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the portal tracts contain large number of chronic inflammatory cells and in some area
these inflammatory cells spill over the limiting plate into nodules of hepatocytes
fibrous bands containing inflammatory cells found